Dott. Stefano Gatti
- f502-c003 Dottorato in Medicina Molecolare
- Dottorato: 27° ciclo
- Matricola: 305360
Contatti
- 116707747
- 116705931
- Chiama gstefanog
- stefano.gatti@unito.it
- Corso Massimo D'Azeglio, 52
10126 Torino
Italy - https://dott-mm.campusnet.unito.it/do/studenti.pl/Show?305360
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Supervisore
Tiziana CrepaldiTesi di dottorato
HUMAN HEALTH: STUDY AND TREATMENT OF TUMORS AND DEGENERATIVE DISEASES WITH NEW APPROACHES DERIVED FROM HUMAN GENOME KNOWLEDGE
Myocyte loss in the ischemically injured mammalian heart often leads to irreversible degenerative cardiac disease. Met, the tyrosine kinase receptor for HGF, controls a genetic program including protection from apoptosis and cell survival.This program is known to play a key role in embryo development, organ regeneration and cancer. In this project we will characterize the HGF effects on the regulation of cardiac genetic pattern in physiological and ischemic condition.We will also treat a cell line of cardiac progenitors and I/R animal models with agonists of Met to stimulate their survival and proliferation. These results can find new therapeutic tools for stimulate endogenous stem cells capable of restoring damaged cardiac tissue.
HGF and c-Met pathophysiological role in mouse heart
The Hepatocyte Growth Factor (HGF) and its tyrosine-kinase receptor c-Met are involved in many physiological and pathological processes including regulation of growth and differentiation in different tissues. Since few information exists about their role in cardiac tissue, using two TetOff bitransgenic conditional mouse models expressing respectively the HGF growth factor and Tpr-Met, the constitutively active oncogenic form of Met receptor, specifically in cardiomyocytes could lead to a better comprehension of the function of HGF and its receptor c-Met in the heart.